期刊
NATURE
卷 478, 期 7367, 页码 76-81出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nature10449
关键词
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资金
- Austrian Academy of Sciences
- Austrian Research Promotion Agency
- SFB Lipotox F30 of the Austrian Science Fund
- NIH [HL088093, RO1 HL086599, EY14005, EY019044]
- Edward N. & Della L. Thome Memorial Foundation
- Research to Prevent Blindness (Wilmer Eye institute)
- Deutsche Forschungsgemeinschaft
- ProRetina Foundation
- Fondation Leducq
- Wynn-Gund Translational Research Acceleration Program Enhanced Research and Clinical Training Award
- National Neurovision Research Institute - Foundation Fighting Blindness
- Macular Degeneration Research Award
- American Health Assistance Foundation
- European Commission
- European Community
- American Heart Association [0630228N]
Oxidative stress and enhanced lipid peroxidation are linked to many chronic inflammatory diseases, including age-related macular degeneration (AMD). AMD is the leading cause of blindness in Western societies, but its aetiology remains largely unknown. Malondialdehyde (MDA) is a common lipid peroxidation product that accumulates in many pathophysiological processes, including AMD. Here we identify complement factor H (CFH) as a major MDA-binding protein that can block both the uptake of MDA-modified proteins by macrophages and MDA-induced proinflammatory effects in vivo in mice. The CFH polymorphism H402, which is strongly associated with AMD, markedly reduces the ability of CFH to bind MDA, indicating a causal link to disease aetiology. Our findings provide important mechanistic insights into innate immune responses to oxidative stress, which may be exploited in the prevention of and therapy for AMD and other chronic inflammatory diseases.
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